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筋炎特異抗体“陰性”筋炎の臨床・分子病理像解析と合併背景免疫の病態への関与の検討

肌炎特异性抗体“阴性”肌炎的临床和分子病理分析及潜在免疫系统参与病理学的研究

基本信息

批准号：
22K07506
负责人：
清水潤
金额：
$ 2.66万
依托单位：
Tokyo University of Technology
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2022
资助国家：
日本
起止时间：
2022-04-01 至 2025-03-31
项目状态：
未结题

项目摘要

本研究のテーマである筋炎特異抗体“陰性”筋炎の病態の解明においては，「複数の背景免疫因子が存在すると臨床病理像はミックスされるか？」という点は，解決すべき疑問である．そこで，2022年度は，免疫介在性壊死性ミオパチー（IMNM）に筋炎特異抗体“陰性”筋炎に出現する膠原病関連自己抗体が合併した場合に，筋病理像に変化が及ぶかを検討した．IMNM連続40例（抗SRP抗体陽性20例，抗HMGCR抗体陽性20例，男性22例，女性18例．平均年齢62歳）を対象とした．合併自己抗体の有無はコマーシャルキットで評価した．病理所見は半定量的指標を用い，HE染色で炎症像，壊死再生像の程度を，免疫組織学的変化は各種免疫染色をおこなった上で染色性を評価した． 17例（42.5%）で合併抗体［SS-A (9), RF (6), AMA-M2 (3), CCP (2), Ku(2), Ro-52(2), Mi2(1), RNP(1), SS-B(1), AChR(1), 重複あり］を認めた．合併抗体の有無で，炎症細胞浸潤の程度，壊死再生線維の頻度には有意差はなかった．一方，免疫組織化学ではMxAの筋線維上の発現は両群で陰性，MHC-classⅡの非壊死筋線維上の発現頻度には有意差はなかったが，合併抗体群においてMHC-classⅠの発現がより広範（筋線維の50％以上）である症例の頻度が高く（p＜0.05），MxAの小血管の発現は合併抗体群で有意に高頻度であった（合併抗体群9/17（53％）　v.s. 非合併群1/23（4％，p<0.001）．以上よりIMNMでは半数近くの症例で，筋炎特異抗体“陰性”筋炎でも認める合併抗体が併存していること，IMNMの筋病理像が合併抗体の存在により影響をうけることが明らかになった．

In this study, the specific antibody of tendonitis was "negative" and the pathological explanation of tendonitis was "multiple background immune factors exist". To solve the problem of. Therefore, in 2022, in cases of immune-mediated lethal myositis (IMNM),"negative" myositis specific antibodies, and collagen disease-related antibodies that are combined, pathological changes in the myositis will be investigated. There were 40 IMNM cases (20 cases were anti-SRP antibody positive, 20 cases were anti-HMGCR antibody positive, 22 cases were male, and 18 cases were female. The average age is 62 years. Merged his antibody has no comment. Pathological findings are semi-quantitative indicators, HE staining, inflammation, degree of death and regeneration, immunohistochemical staining, and various immunostaining. Seventeen cases (42.5%) had combined antibodies [SS-A (9), RF (6), AMA-M2 (3), CCP (2), Ku(2), Ro-52(2), Mi2(1), RNP(1), SS-B(1), AChR(1), repeat]. The presence or absence of antibodies, the degree of inflammatory cell infiltration, the frequency of death and regeneration, and the frequency of death and regeneration are intentionally different. On the other hand, immunohistochemical staining showed that MxA was negative on muscle lines, MHC-class II was significantly more frequent on non-muscle lines, MHC-class I was significantly more frequent (p<0.05), and MxA was significantly more frequent in small vessels than in pooled antibody groups (9/17 (53%) v.s. 1/23 (4%, p<0.001). In nearly half of the cases mentioned above, the specific antibody of tendon inflammation "negative" tendon inflammation is recognized as coexisting antibodies, and the pathological image of tendon inflammation is affected by the presence of coexisting antibodies.